Европейские и британские рекомендации требуют междисциплинарного подхода к лечению псориаза и болезни Крона

Current European and UK guidance incorporates comorbidity assessment and, where appropriate, communication between dermatology and gastroenterology into treatment planning Plaque psoriasis and Crohn’s disease are chronic immune-mediated inflammatory diseases affecting anatomically distinct barrier tissues. Psoriasis is characterised by well-demarcated, erythematous, scaly plaques arising from immune-driven keratinocyte hyperproliferation; Crohn’s disease is a relapsing, transmural inflammatory disorder that may involve any part of the gastrointestinal tract. Their co-occurrence is supported by epidemiological, genetic and immunological evidence, but the diseases are not interchangeable expressions of a single process. Tissue-specific immune regulation remains central to clinical assessment and treatment selection. Against this background, this report examines the intersecting biology of plaque psoriasis and Crohn’s disease, with particular consideration of the IL-12/23 pathway, while placing this pathway within the broader therapeutic landscape relevant to both conditions. For dermatologists, gastrointestinal symptoms may identify previously unrecognised inflammatory bowel disease (IBD) or affect the suitability of a psoriasis therapy. For gastroenterologists, cutaneous lesions may represent conventional psoriasis, an IBD-associated dermatosis or a paradoxical psoriasiform eruption during tumour necrosis factor (TNF) inhibitor treatment. Current European and UK guidance incorporates comorbidity assessment and, where appropriate, communication between dermatology and gastroenterology into treatment planning. A bidirectional epidemiological association A 2018 systematic review and meta-analysis of five case-control or cross-sectional studies and four cohort studies, comprising 7,794,087 participants, found significantly increased odds of Crohn’s disease among patients with psoriasis (odds ratio [OR] 1.70; 95 per cent confidence interval [CI] 1.20–2.40). Cohort analyses also found an increased risk of incident Crohn’s disease (risk ratio 2.53; 95 per cent CI 1.65–3.89). ECCO’s guideline on extraintestinal manifestations reports psoriasis among the inflammatory and autoimmune skin disorders associated with IBD, while distinguishing it from reactive dermatoses such as erythema nodosum and pyoderma gangrenosum. In established psoriasis, persistent diarrhoea, abdominal pain, rectal bleeding, weight loss, nocturnal symptoms or perianal disease warrant consideration of IBD and further assessment. In established Crohn’s disease, new scaly plaques, scalp or nail involvement, flexural or palmoplantar disease, and associated joint symptoms should be documented. Diagnosis of suspected IBD is based on clinical symptoms together with laboratory tests, endoscopy, histology and imaging; symptom screening alone is insufficient. Shared immunological architecture Both diseases arise through interactions among genetic susceptibility, epithelial-barrier biology, innate immunity and adaptive immune responses. Genome-wide association studies have identified overlap in immune-regulatory regions, including loci related to IL-23 signalling; IL23R variants have been associated with both IBD and psoriasis. Overlap at pathway level does not imply identical risk alleles or identical cellular effects in skin and bowel. TNF is an established inflammatory mediator in both conditions. The IL-12/IL-23 cytokine family provides a further point of intersection. IL-12 and IL-23 share the p40 subunit but have distinct partner subunits and biological effects. IL-12 supports type 1 immune responses, whereas IL-23 promotes the persistence and pathogenic functions of type 17 cells and other IL-17-producing populations. In psoriatic skin, dendritic-cell-derived IL-23, type 17 cytokines and keratinocyte responses form an amplifying inflammatory circuit. In Crohn’s disease, IL-23-responsive lymphocyte populations participate in chronic intestinal inflammation within a system also shaped by microbial exposure, epithelial integrity and mucosal repair. Convergence does not remove tissue specificity The IL-17 pathway illustrates the limits of direct extrapolation between organs. IL-17A inhibition produces high levels of skin clearance in plaque psoriasis and is represented in current psoriasis guidelines. However, IL-17-pathway blockade has not demonstrated therapeutic efficacy in Crohn’s disease. European psoriasis guidance advises against IL-17 inhibitors in active Crohn’s disease. Product-specific SmPC recommendations should be considered and gastroenterology input sought where IBD is present. This divergence is consistent with the protective functions attributed to IL-17 signalling in intestinal epithelial defence and barrier maintenance, alongside its inflammatory activity in other settings. Therapeutic effects across the two diseases vary according to the pathway and individual agent. Selected IL-23 inhibitors and IL-12/23 p40 inhibition have demonstrated efficacy in both plaque psoriasis and Crohn’s disease, while particular TNF inhibitors also have established roles in both conditions. These differences require pathway-specific, agent-specific and indication-specific appraisal rather than extrapolation based solely on cytokine nomenclature. Clinical phenotyping when both disease domains are relevant The temporal relationship between intestinal disease, skin disease and treatment is material. Psoriasis may precede Crohn’s disease, emerge independently after the IBD diagnosis, or appear during TNF inhibitor therapy. Anti-TNF-associated eruptions include plaque, scalp, palmoplantar pustular and inverse patterns. Dermatological assessment, with biopsy where clinically indicated, may be required when morphology is atypical or the diagnosis is uncertain. ECCO recommends multidisciplinary management according to IBD activity, eruption severity and the indication for the causative treatment. Mild eruptions may sometimes be treated topically without withdrawing an otherwise effective IBD therapy, whereas severe or refractory disease may require treatment modification. Assessment should also identify psoriatic arthritis, smoking, obesity and cardiometabolic disease, infection risk, vaccination status, pregnancy plans and previous malignancy. In Crohn’s disease, relevant features include disease location, stricturing or penetrating behaviour, perianal disease, prior resection, objective inflammatory activity and previous advanced-therapy exposure. In psoriasis, body surface area, Psoriasis Area and Severity Index, Dermatology Life Quality Index, difficult-to-treat sites and joint disease contribute to therapeutic assessment. Treatment across skin and gut The overlapping treatment landscape includes monoclonal antibodies directed against TNF, the shared IL-12/23 p40 subunit and the IL-23 p19 subunit. Several agents within these pathways have therapeutic roles across the two disease domains, but efficacy and regulatory authorisation remain agent-specific. This distinction is particularly important within the TNF inhibitor class: monoclonal antibodies such as infliximab and adalimumab have established roles in both plaque psoriasis and Crohn’s disease, whereas etanercept is indicated in plaque psoriasis only. Within the selective IL-23p19 inhibitor class, EU-authorised indications vary by molecule. Risankizumab and guselkumab are authorised for both moderate-to-severe plaque psoriasis and moderately-to-severely active Crohn’s disease. Tildrakizumab is authorised for plaque psoriasis but not Crohn’s disease, whereas mirikizumab is authorised for Crohn’s disease but not plaque psoriasis. The applicable Summary of Product Characteristics (SPC) should therefore be checked when treatment is selected. The 2024 European Crohn’s and Colitis Organisation (ECCO) treatment guideline recommends infliximab, adalimumab, ustekinumab and risankizumab (all also indicated for plaque psoriasis), and vedolizumab and upadacitinib for induction and maintenance in moderate-to-severe Crohn’s disease. EuroGuiDerm lists conventional systemic agents, biologics and small molecules for plaque psoriasis and provides a comorbidity-based decision grid that distinguishes among therapies according to their suitability in patients with concomitant Crohn’s disease. Treatment selection should therefore reflect the activity and therapeutic requirements of both diseases, previous treatment exposure, relevant comorbidities, and the evidence and authorised indications for the individual agent. The British Association of Dermatologists likewise requires relevant comorbidity, including IBD, to inform biologic selection. For each advanced therapy, prescribing should follow the authorised SPC, including indication, dosing, contraindications, warnings and monitoring requirements. Cross-specialty coordination A dermatologist assessing possible IBD should establish symptom duration, bleeding, weight change, nocturnal symptoms, family history and perianal features, and arrange gastroenterology assessment where indicated. Faecal calprotectin is an important non-invasive marker of intestinal inflammation and can support the evaluation of suspected IBD, but diagnosis requires integration of clinical, laboratory, endoscopic, histological and imaging findings. A gastroenterologist assessing a new eruption should document morphology, distribution, timing relative to therapy and associated nail or joint findings, and seek dermatology review when the diagnosis or treatment consequence is uncertain. Before advanced therapy, both specialties should address infection screening, vaccination and contraindications in accordance with the selected medicine’s SPC and the relevant disease guideline. During treatment, response should be measured in the relevant organ using validated clinical and objective outcomes. ECCO diagnostic and monitoring guidance emphasises that symptoms alone may not reflect inflammatory activity and incorporates biomarkers, endoscopy and cross-sectional imaging according to the clinical setting. Shared documentation of treatment history, therapeutic response and adverse events reduces the risk of conflicting changes to systemic therapy. Conclusion Plaque psoriasis and Crohn’s disease show a reproducible epidemiological association and intersect at TNF- and IL-23-related immune pathways. Their biology nevertheless remains organ-specific, as demonstrated most clearly by the different clinical effects of IL-17 inhibition in skin and intestine. Current European and UK guidance supports comorbidity-sensitive, agent-specific treatment selection and cross-specialty management when the conditions coexist or when treatment-associated psoriasiform disease is suspected. References available on request.